18ß-Glycyrrhetinic acid inhibits adipogenic differentiation and stimulates lipolysis.

18ß-Glycyrrhetinic acid (18ß-GA) obtained from the herb liquorice has various pharmacological properties including anti-inflammatory and anti-bacterial activities. However, potential biological anti-obesity activities are unclear. In this study, novel biological activities of 18ß-GA in the adipogenesis of 3T3-L1 preadipocytes and in lipolysis of differentiated adipocytes were identified. Mouse 3T3-L1 cells were used as an in vitro model of adipogenesis and lipolysis, using a mixture of insulin/dexamethasone/3-isobutyl-1-methylxanthine (IBMX) to induce differentiation. The amount of lipid droplet accumulation was determined by an AdipoRed assay. The expression of several adipogenic transcription factors and enzymes was investigated using real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. 18ß-GA dose-dependently (1-40 µM) significantly decreased lipid accumulation in maturing preadipocytes. In 3T3-L1 preadipocytes, 10 µM of 18ß-GA down-regulated the transcriptional levels of the peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α and adiponectin, which are markers of adipogenic differentiation via Akt phosphorylation. Also, in differentiated adipocytes, 18ß-GA increased the level of glycerol release and up-regulated the mRNA of hormone-sensitive lipase, adipose TG lipase and perilipin, as well as the phosphorylation of hormone-sensitive lipase at Serine 563. The results indicate that 18ß-GA alters fat mass by directly affecting adipogenesis in maturing preadipocytes and lipolysis in matured adipocytes. Thus, 18ß-GA may be useful for the treatment of obesity.

Branching pattern of aortic arch in the Korean water deer.

This study examined the branching pattern of the aortic arch and its major branches in Korean water deer (Hydropotes inermis argyropus, Heude, 1884). Silicone casts were taken from the vessels of 23 carcasses (male 14, female 9) with body weights ranging from 1.3-16.0 kg through a retrograde injection into the abdominal aorta. The findings were compared with those from other domestic ruminants. Only the brachiocephalic trunk (Bct) branched from the aortic arch in all carcasses. In 19 of the 23 cases, the Bct branched into the left subclavian artery (LSb), the left common carotid artery (LCc), and then trifurcated into the right common carotid artery (RCc), right costocervical trunk (RCct) and right subclavian artery (RSb). The subclavian artery (Sb) branched into the costocervical trunk (in left), internal thoracic artery (It), and superficial cervical artery (Sc) in that order, and continued as the axillary artery. Instead of separated carotid arteries, the bicarotid trunk from the Bct was observed in only three males and one female. Two of these males had different branching orders of the It and Sc from the Sb in one or both sides. The other male had a RCct from the RSb. The left costocervical trunk (LCct) arose from the LSb in all cases, and branched into the highest intercostal artery, the dorsal scapular artery, and the deep cervical arteries in that order, and continued as the vertebral artery. In 22 cases, the RCct branched directly from the Bct at the same point in which the RCc (or bicarotid trunk) and RSb separated. The artery branching pattern from the RCct was similar to that of the LCct. These results suggest that the Korean water deer has a Bct with different branching patterns from those of domestic ruminants.

Caffeine prevents human prion protein-mediated neurotoxicity through the induction of autophagy.

The human prion protein (PrP) fragment PrP(106­126) possesses the majority of the pathogenic properties associated with the infectious scrapie isoform of PrP, known as PrPSc. The accumulation of PrPSc in the brain of humans and animals affects the central nervous system. Recent epidemiological studies have suggested that caffeine, one of the major components of coffee, exerts protective effects against the development of neurodegeneration. However, the protective effects of caffeine against prion disease have not been reported to date. In this study, we therefore investigated the effects of caffeine on PrP-mediated neurotoxicity. The protein expression of the autophagosomal marker, LC3-II, was increased by caffeine in a dose-dependent manner, and the autophagy induced by caffeine protected the neuronal cells against PrP(106­126)­induced cell death. On the contrary, the downregulation of LC3-II using the autophagy inhibitors, 3-methyladenine (3-ΜΑ) and wortmannin, prevented the caffeine-mediated neuroprotective effects. To the best of our knowledge, the present study provides the first evidence that treatment with caffeine protects human neuronal cells against prion­mediated neurotoxicity and these neuroprotective effects are mediated by caffeine-induced autophagy signals. Our data suggest that treatment with caffeine may be a novel therapeutic strategy for prion peptide­induced apoptosis.